Malignant murine erythroleukemia (MEL) cells which continuously produce Friend virus, can be induced to differentiate along the erythroid pathway by diverse biological agents including DMSO, butyrate, SeO2, DNA inhibitors, and certain antibiotics. Low molecular weight aldehydes, ketones, organic acids, ethers, and alcohols are also potent inducers. The activity of these latter compounds suggest that exogenous carbonyl compounds may provide the initiation signal for erythroid differentiation in MEL cells. When a variety of different inducers stimulate hemoglobin synthesis in MEL cells, intracellular porphyrin production which is mostly protoporphyrin, also increases. However, extracellular porphyrin production on a cellular basis is elevated 10-20 times that in the cells. This phenomenon may serve as a molecular model for the disease symptoms of human porphyria. Succinylacetone, a potent inhbitor of heme biosynthesis, was shown to inhibit gamma aminolevulinic acid dehydratase, the second enzyme of the heme pathway, at concentrations of 10 to the 8th power M and higher. The compound inhibited the induction of erythroid differentiation in MEL cells by DMSO and butyrate. MEL cell multiplication was inhibited by succinylacetone when cellular heme levels were reduced to 1/6 the level found in untreated dividing cells. Succinylacetone shows promise as a chemotherapeutic agent against fast-growing tumor cells by ultimately affecting their respiration and protein synthesis.